Martin S E, Lenhard S D, Schmarkey L S, Offenbacher S, Odle B M
Department of Medicine (Cardiology), Carlyle Fraser Heart Center, Crawford Long Hospital of Emory University, Atlanta, Georgia.
Am J Physiol. 1993 May;264(5 Pt 2):H1438-46. doi: 10.1152/ajpheart.1993.264.5.H1438.
Adenosine may mediate coronary vasodilation during work-related hyperemia and during ischemia. We tested whether adenosine blockade with 8-p-sulfophenyltheophylline (PSPT) prevented dobutamine-induced hyperemia or magnified the reductions in flow due to vasopressin. Control (n = 8) and test (n = 7) dogs received paired infusions of dobutamine (70 micrograms/min iv for 5 min). Test dogs received PSPT (10 mg/kg iv) between doses. In both groups, paired infusions elicited comparable increases in oxygen consumption. However, in test dogs, the hyperemia was reduced significantly. Thus adenosine mediates the hyperemia of dobutamine. Separately, control dogs (n = 9) received vasopressin (0.6 microgram ic over 5 min); test dogs (n = 7) received PSPT before vasopressin. Vasopressin maximally increased coronary resistance by 3 min; effects were gone by 10 min. With PSPT, coronary resistance was increased further and remained high beyond 10 min. Thus adenosine-mediated vasodilation moderates the severity and duration of ischemia. These results indicate the importance of adenosine in mediating coronary flow during increased demand and reduced supply.
腺苷可能在与工作相关的充血期间以及缺血期间介导冠状动脉扩张。我们测试了用8-对磺基苯甲基黄嘌呤(PSPT)阻断腺苷是否能预防多巴酚丁胺诱导的充血,或放大血管加压素导致的血流减少。对照组(n = 8)和试验组(n = 7)犬接受多巴酚丁胺的配对输注(静脉注射70微克/分钟,持续5分钟)。试验组犬在两次剂量之间接受PSPT(静脉注射10毫克/千克)。在两组中,配对输注引起的耗氧量增加相当。然而,在试验组犬中,充血明显减少。因此,腺苷介导了多巴酚丁胺引起的充血。另外,对照组犬(n = 9)接受血管加压素(5分钟内0.6微克冠状动脉内注射);试验组犬(n = 7)在血管加压素之前接受PSPT。血管加压素在3分钟时使冠状动脉阻力最大程度增加;10分钟时作用消失。使用PSPT时,冠状动脉阻力进一步增加,并在10分钟后仍保持在高位。因此,腺苷介导的血管舒张减轻了缺血的严重程度和持续时间。这些结果表明腺苷在需求增加和供应减少期间介导冠状动脉血流中的重要性。